Knockdown of Long Non-coding RNA LINC00473 Protects CHON-001 Cells against Interleukin-1β-Induced Cell Injury

Abstract

Osteoarthritis is a chronic joint disease with high prevalence. However, effective treatment options for OA are still lacking. It was previously reported that LINC00473 was upregulated in patients with OA and upregulated LINC00473 might associated with the progression of OA; however, the role of LINC00473 in OA remains to be investigated. CHON-001 human chondrocyte cells stimulated with 10 ng/ml IL-1β were utilized to mimic OA in vitro. Protein expression, cell apoptosis and cell proliferation of CHON-001 cells were investigated by western blot, Annexin V and PI double staining, cell counting-8 kit assay and immunofluorescence staining respectively. The result indicated IL-1β triggered viability decrease and apoptosis in CHON-001 cells, which was alleviated by LINC00473 knockdown. Meanwhile, IL-1β-induced upregulation of cleaved caspase 3 and Bax were ameliorated by LINC00473 knockdown. Likewise, IL-1β-induced downregulation of XIAP was alleviated by LINC00473 knockdown. In addition, LINC00473 knockdown protected CHON-001 cells against IL-1β by inhibiting the methylation of LIM mineralization protein-1 (LMP)-1 gene. Moreover, JNK/NF-κB signaling pathway was proved to be involved in the cell protective effect of LINC00473 knockdown in IL-1β treated CHON-001 cells. Taken together, LINC00473 knockdown defended CHON-001 cells from IL-1β induced cell injury via inhibition of the methylation of LMP-1. Thus, LINC00473 might possibly act as a novel therapeutic target for OA.

LIM mineralization protein‑1 inhibits IL‑1β‑induced human chondrocytes injury by altering the NF‑κB and MAPK/JNK pathways

“…IL-1β-stimulated chondrocytes have been used to mimic articular cartilage injury in vitro (14). IL-1β-stimulated CHON-001 cells have been widely used as an in vitro model to study OA (15)(16)(17)(18).…”